Decreases in H2A monoubiquitination in the amygdala constrain fear memory formation
- 1School of Animal Sciences, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061, USA
- 2School of Neuroscience, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061, USA
- Corresponding author: tjjarome{at}vt.edu
Abstract
Evidence suggests a role for monoubiquitination of histone H2B, a regulator of increased gene transcription, in memory formation. However, whether monoubiquitination of histone H2A (H2Aubi), a transcriptional repressor, is involved in memory formation has not been explored. We found global and gene-specific decreases in H2Aubi in the amygdala following fear conditioning. H2Aubi decreased at Pten, an inhibitor of PI3K–AKT–mTOR signaling, which occurred concurrently with increases in PTEN expression. CRISPR–dCas9 mediated upregulation of the H2Aubi ligase, Ring1b, in the amygdala enhanced contextual memory. These results suggest that decreases in transcriptionally repressive H2Aubi in the amygdala functions to constrain fear memory strength.
Footnotes
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[Supplemental material is available for this article.]
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Article is online at http://www.learnmem.org/cgi/doi/10.1101/lm.054092.125.
- Received January 17, 2025.
- Accepted February 26, 2025.
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